Varicella zoster virus (VZV) is the cause of chickenpox in children, usually a mild, self-limiting disease. However, VZV, a member of the herpes family of viruses, remains in a latent form in the neural cells of the host. Reactivation of the latent virus in middle-aged adults causes herpes zoster, which is the second clinical manifestation of the infection. Common ocular complications of herpes zoster are chronic corneal ulceration, uveitis, glaucoma and cataracts. Corneas scarred by zoster heal very poorly, and can rarely be successfully replaced by transplant surgery. Therefore, understanding the pathogenesis of zoster infection, and development of a reproducible animal model of the disease are high-priority research objectives of the National Eye Institute. Unfortunately, the clinical symptoms of varicella zoster infection cannot be reproduced in common laboratory animals. To achieve these goals, we plan to initiate studies of varicella virus infection in squirrel monkeys, an inexpensive, readily- available non-human primate. Simian varicella virus infection of monkeys produces disease which very closely resembles varicella zoster infection in humans. Also, the genome of the human and simian virus are very similar, with at least 70% DNA homology. Since the varicella viruses are highly host-specific, they must first be adapted for growth in cultures of squirrel monkey cells in vitro. This will be accomplished by repetitiously passing the virus from one culture of squirrel monkey cells to another until it acquires the ability to grow well in the new host cells. The host-adapted virus strain will then be used to inoculate squirrel monkeys to determine its pathogenicity. The successful demonstration of varicella infection in squirrel monkeys will be of considerable value for future studies of the pathogenesis, immunology and antiviral therapy of varicella virus infections both in humans and other primates.